Recurrent chromosome changes in 62 primary gastric carcinomas detected by comparative genomic hybridization

Guan, Xin Yuan; Fu, Song; Xia, Jian Chuan; Fang, Yan; Sham, Jonathan S. T.; Du, Bao Dong; Zhou, Hang; Lu, Song; Wang, Bai Qiu; Lin, Yi; Liang, Qiaoli; Li, Xiao Ming; Du, Bo; Ning, Xuan; Du, Jin Rong; Li, Pu; Trent, Jeffrey M.

doi:10.1016/s0165-4608(00)00306-x

Cited by 50 publications

(52 citation statements)

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“…Previous CGH studies of gastric cancers yielded similar results. Moreover, several CGH studies identified the 20q region as the most frequent site of gain of DNA in gastric [29][30][31][32]34,35,39 Amplification at 20q has been reported in several cancers, such as colon cancer, 40 pancreatic cancer, 41,42 lung adenocarcinoma, 43 ovarian carcinoma, 44 and osteosarcoma. 45 In our study, gain of 20q was detected in 71 cases (70%) and was associated with the pattern of the cancer-stroma 51 and CYP24 (20q13.2).…”

Section: Discussionmentioning

confidence: 99%

“…Deletion of 19p has been reported in gastric cancer, and chromosome 19p might include tumor suppressor genes that play an important role in the development and progression in gastric cancers. 39 Recently, the gene for antizyme (OAZ1), a negative regulator of cellular polymines, is mapped to 19p13.3, where frequent allelic imbalance is observed in ovarian cancer. But it was reported that one or more tumor suppressor genes other than OAZ1 gene exist on 19p13.3.…”

Section: Genetic Alterations In Gastric Cancermentioning

confidence: 99%

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Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

et al. 2004

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Gastric cancer is one of the most common cancers. Molecular events in the carcinogenesis of gastric cancer remain, however, largely undefined. We investigated changes in DNA copy number in 102 gastric cancers by CGH. We found changes in DNA copy number in all cases, with frequent (^30% of patients) gains at 20q, 8q, 20p, 7q, 17q, 5p, and 13q. Frequent (^20%) losses were found at 19p, 18q, 5q, 21q, 4p, 4q, 15q, and 17p. The mean number of total alterations was significantly lower in grade 3 and scirrhous-type carcinomas (10.81 in grade 3 vs 13.98 in grade 1 and grade 2, 9.31 in scirrhous-type vs 13.18 in medullary-and intermediate-type). The mean number of losses and total alterations were higher in tumors at pT2, pT3 and pT4 (4.68 and 12.77 in pT2, pT3, and pT4 vs 2.55 and 9.22 in pT1). The mean number of losses was higher in carcinomas with lymph node metastasis (4.83). The mean number of gains and total alterations were higher in carcinomas with venous invasion (8.44 and 13.28). Several chromosomal alterations were linked in a statistically significant manner to specific clinicopathological parameters. Gain of 17q, 20p, and 20q and loss of 4p were associated with the pattern of the cancer-stroma relationship; loss of 18q was associated with pT category; gain of 5p was associated with pN category; loss of 4q and loss of 21q were associated with lymphatic invasion; gain of 7p and loss of 4q and 18q were associated with venous invasion; and loss of 18q was associated with pathological stage. These data suggest that gain of 20q and loss of 18q might play an important role in the development and progression of gastric cancer. Moreover, some genes on 20q and 18q might be target genes of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Genetic Alterations In Gastric Cancermentioning

confidence: 99%

Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

et al. 2004

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“…These mechanisms are to a large extent caused by genetic changes that occur at the chromosomal level. Therefore, DNA copy number profiling is a sensible approach for genotyping in gastric cancer (Kokkola et al, 1998;Sakakura et al, 1999;Guan et al, 2000;Grieken van et al, 2000;van Dekken et al, 2001;Wu et al, 2001). Furthermore, while DNA copy number changes detected by microarray-based CGH are completely attributable to the tumour cells, gene expression profiles of tumours will be influenced by stress responses.…”

Section: Discussionmentioning

confidence: 99%

Genomic profiling of gastric cancer predicts lymph node status and survival

et al. 2003

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Gastric carcinogenesis is driven by an accumulation of genetic changes that to a large extent occur at the chromosomal level. We analysed the patterns of chromosomal instability in 35 gastric carcinomas and their clinical correlations. With microarray competitive genomic hybridization, genomewide chromosomal copy number changes can be studied with high resolution and sensitivity. A genomewide scanning array with 2275 BAC and P1 clones spotted in triplicate was used. This array provided an average resolution of 1.4 Mb across the genome. Patterns of chromosomal aberrations were analysed by hierarchical cluster analysis of the normalized log 2 tumour to normal fluorescence ratios of all clones, and cluster membership was correlated to clinicopathological data including survival. Hierarchical cluster analysis revealed three groups with different genomic profiles that correlated significantly with lymph node status (P ¼ 0.02). Moreover, gastric cancer cases from cluster 3 showed a significantly better prognosis than those from clusters 1 and 2 (P ¼ 0.02). Genomic profiling of gastric adenocarcinomas based on microarray analysis of chromosomal copy number changes predicted lymph node status and survival. The possibility to discriminate between patients with a high risk of lymph node metastasis could clinically be helpful for selecting patients for extended lymph node resection.

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“…As the target areas, we selected seven microsatellite loci (D8S530, D8S1724, D8S1801, D16S3140, D16S3026, D20S911, and D20S185) in three chromosomal arms (8q, 16q, and 20q) and one gene-specific locus (ZNF217). Those selected loci had previously been frequently reported to be abnormal in DNA copy numbers by CGH analysis (22)(23)(24)(25)(26). On this basis of the TaqMan PCR system performed on the ABI 7700 instrument (Applied Biosystems, Foster City, CA), we used internal probes carrying donor (6-carboxyfluorescein) and acceptor (6-carboxytetramethylrhodamine) fluorescence molecules complementary to CA repeats in the micosatellite markers and to a gene-specific oligomer in the gene-specific marker (Table 2).…”

Section: Methodsmentioning

confidence: 99%

“…Recently, comparative genomic hybridization (CGH) enables detection of the recurrent abnormal regions in the DNA copy number encoding new genes that contribute to carcinogenesis and the progression of stomach cancer. Several reports dealing with CGH analysis on stomach cancer disclosed gains of 1q, 7q, 8q, 17q, and 20q and losses of 1p, 4q, 5q, 16q, and 17p (21)(22)(23)(24)(25). However, the resolution of CGH is not high enough to enable the precise detection of copy number aberrations limited to a pinpoint region within a chromosomal arm.…”

Section: Introductionmentioning

confidence: 99%

Comparative Study between DNA Copy Number Aberrations Determined by Quantitative Microsatellite Analysis and Clinical Outcome in Patients with Stomach Cancer

Suzuki

Egami²,

Sasajima³

et al. 2004

Clinical Cancer Research

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Purpose: We detected the relative DNA copy numbers (RCNs) at target loci in patients with stomach cancer with quantitative microsatellite analysis. We additionally clarified the relationship between DNA copy number aberrations and the clinical outcome of the patients.Experimental Design: Fresh frozen samples were obtained from 30 patients who had undergone surgery for stomach cancer. Seven microsatellite loci in chromosomes 8q, 16q, and 20q and one gene-specific locus (ZNF217) were selected as the target loci. The DNA copy number was obtained relatively to a pooled reference consisting of six microsatellite primer sets selected from the regions where few aberrations have been reported in comparative genomic hybridization analysis. On the basis of the TaqMan PCR system, the internal probes used were carrying donor (6-carboxyfluorescein) and acceptor (6-carboxytetramethylrhodamine) fluorescent molecules complementary to CA repeats in the microsatellite markers and to one gene-specific oligomer in the gene-specific marker.Results: Chromosome 8q gain, 20q gain, and 16q loss were detected in 18 (60.0%), 8 (26.7%), and 13 (43.3%) cases, respectively. Gains in the RCNs of D8S1801 and D8S1724 were most frequently found (36.7%). There was a significant correlation between the loss of D16S3026 and reduced survival duration (P ‫؍‬ 0.0158), and the simultaneous aberrations of D8S1801 gain and D16S3026 loss (double marker positive) was significantly associated with reduced survival duration (P ‫؍‬ 0.0008). According to Cox proportional hazards model, the double marker positive was a significant and independent factor indicating an unfavorable prognostic factor (relative risk, 17.176; 95% confidence interval, 2.782-106.026; P ‫؍‬ 0.0022).Conclusion: RCN aberrations in tumor tissues determined by quantitative microsatellite analysis enable identification of the prognostic factors that correlate with clinical outcome of the patients with stomach cancer.

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Recurrent chromosome changes in 62 primary gastric carcinomas detected by comparative genomic hybridization

Cited by 50 publications

References 19 publications

Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

Genetic alterations in 102 primary gastric cancers by comparative genomic hybridization: gain of 20q and loss of 18q are associated with tumor progression

Genomic profiling of gastric cancer predicts lymph node status and survival

Comparative Study between DNA Copy Number Aberrations Determined by Quantitative Microsatellite Analysis and Clinical Outcome in Patients with Stomach Cancer

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